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Escherichia coli O157:H7 remains a challenge for the beef industry. Research has shown carcass
interventions consisting of hot water sprays paired with organic acid rinses to be highly effective at
reducing pathogen loads on carcasses. Nevertheless, the mechanisms by which hot water and
organic acid interventions interact to inhibit foodborne pathogens remain unclear. Hot water is
thought to function primarily by physically dislodging loosely attached pathogens, thermal
inactivation, or some combination thereof. A widely accepted theory of organic acid action states
that at reduced environmental pH, the protonated acid penetrates the bacterium�s interior. This
consequently induces a cascade of microbial responses designed to ultimately restore pH balance to
the pathogen interior. At sufficient acid levels, the cell will be forced to repeatedly expel protons at
the cost of energy reserves. This model has been criticized as too simplistic in its assertion that
antimicrobial activity results only by acidification of the bacterium interior. Accumulation of
deprotonated acid in the cellular interior is thought to play a major role in the inhibition of cells by
alkalinizing the cell and inhibiting synthesis of macromolecules. <P>
The purpose of this research study
was to determine the extent to which exposure to hot water would result in degradation to the outer
membrane of E. coli O157:H7 and ultimately influence L-lactic acid inhibition of the pathogen.
Findings: Exposure of E. coli O157:H7 to increasing temperatures for increasing intervals resulted in
statistically greater inactivation of the pathogen via hot water. Log reductions ranged from
approximately 3.0-7.0 log cycles, dependent upon exposure temperature and duration of 3 exposure.
Increased exposure to heat produced significant increases in hydroperoxides from E. coli O157:H7
membrane lipids. No detectable surviving E. coli O157:H7 were recovered on microbiological
medium following exposure to any experimental heating protocol and organic acid. Hot watertreated cells did not accumulate significant amounts of organic acid anion, presumably due to
significant degradation to outer membrane lipids.